Liver failure Flashcards
Give 5 functions of the liver and what can occur if they go wrong.
- Produce albumin - hypoalbuminaemia/ ascites
- Regulate excess oestrogen - gynecomastia in men
- Produce clotting factors except VII - easy bruising
- Regulate bilirubin - pruritus (itching)/ jaundice
- Store glycogen, plays role in glycogenesis - hypoglycaemia.
(PTS)
How does liver disease lead to encephalopathy?
- It plays a key role in the urea cycle. If diseased, ammonia builds up and crosses the blood brain barrier, causing hepatic encephalopathy.
How does liver disease lead to spontaneous bacterial peritonitis?
The liver protects against infection via the reticuloendothelial system (kupffer cells). If diseased, the body is prone to infection such as spontaneous bacterial peritonitis.
Define acute liver failure and acute-on-chronic liver failure.
Acute = Liver failure occurs suddenly in previously healthy liver.
Acute- on-chronic = as a result of decompensation of chronic liver disease (OHCM)
What is fulminant liver failure?
Fulminant = sudden or severe onset.
Clinical syndrome resulting from massive necrosis of liver cells, leading to severe impairment of liver function. It can be acute or acute-on-chronic.
What is hyperacute fulminant hepatic failure?
Encephalopathy within 7 days of onset of jaundice
What is acute fulminant hepatic failure?
Within 8-28 days of onset of jaundice.
What is subacute fulminant hepatic failure?
Within 5-26 weeks of onset of jaundice.
Give 3 causes of acute liver injury.
- Viral (hep A, B; EBV)
- Drugs
- Alcohol
- Vascular
- Obstruction
- Congestion
(lecture 22.1.18)
Give 3 causes of chronic liver injury.
- Alcohol
- Viral (hep B, C)
- Autoimmune
- Metabolic (iron, copper)
(Lecture 22.1.18)
Give 3 clinical signs of fulminant hepatic failure.
Encephalopathy - confusion, drowsiness, irritability
Asterixis: flapping hands when flexed back
jaundice
sepsis presentation - tachycardia, tachypnoea
Describe the management of fulminant hepatic failure.
Lactose for encephalopathy
Supportive treatment
Admit to ICU if severe.
Describe the pathophysiology of paracetamol induced FHF.
The sulfate and glucuronide pathways become saturated, so paracetamol is shunted to the cytochrome P450 system to produce NAPQI. This uses up glutathione stores that are used to metabolise NAPQI into harmless substances. Build-up of NAPQI damages liver.
Describe the management of paracetamol induced FHF.
- N Acetyl Cysteine (NAC) - replenishes glutathione and aids excretion of NAPQI.
- Gastric decontamination using activated charcoal.
- Supportive treatment of coagulation defects, fluid electrolyte and acid-base balance, hypoglycaemia etc.
Consider emergency liver transplant
Give 3 indicators of emergency liver transplant.
Late presentation (NAC is less effective >24h)
pH <7.3
PTT >70 sec
Serum creatinine >300micromol/l
